Pharmaceutical interests in the UK are ignoring new scientific
research that shows the insecticide used in the UK government's own warble-fly
campaigns triggered the surge of 'Mad Cow' disease.

Latest experiments by Cambridge University prion specialist,
David R. Brown, have shown that manganese bonds with prions to cause BSE.
Other researchers unpublished work shows that prions in the bovine spine
-along which insecticides are applied- can be damaged by ICI's Phosmet
organophosphate(OP) insecticide -causing the disease.

British scientists have led the current theory that an
infectious prion in bonemeal fed to cattle causes bovine spongiform disease
(BSE). Infectious prions are also claimed to cause new variant Creutzfeld-Jakob
Disease (CJD) in humans -from ingesting beef. But the infectious prion
theory serves to obscure a tragic chemical poisoning scandal behind the
majority of BSE cases.

The new work proves that the prions can bond with manganese
in animal feeds or mineral licks. These manganese prions cause the eurological
degeneration seen in BSE. By a similar process, prions in human brains
are damaged by lice lotions containing organophosphate. This can result
in neurological diseases like CJD and Alzheimers -later in life.

Many might be surprised to hear that organophosphates
were developed by Nazi chemists during the course World War Two, as a chemical
weapon nerve agent. One formulation of the insecticide -Maneb, or Mancozeb-
actually contains manganese in addition to organophosphate.

The marginalised research has devestating financial implications
for ICI. It would provide a firm basis for litigants -who could include
CJD sufferers, farmers across the world, and the spouses and families of
the many British farmers who committed suicide during this BSE debacle.

Phosmet organophosphate has been used at high doses in
British warble fly campaigns. In 1996, ICI subsidiary Zeneca sold the phosmet
patent to a PO Box company in Arizona called Gowan -just one week before
the UK government admitted to a link between BSE and nvCJD.

The politically well-connected British pharmaceuticals
group, ICI has the financial and political clout to block research into
any cause other than the infective model. Indeed no substantive alternative
research has been done. British BSE disease management and research bodies
have taken decisions that do not seem guided by spirited scientific enquiry.
Mysterious prions that jump species is the preferred research arena.

Scientist and organic farmer, Mark Purdey gave evidence
to the UK BSE inquiry, that warble fly insecticide was the cause of the
disease. The scientist wheeled out to rubbish Purdy's evidence -Dr. David
Ray, later turned out to have been receiving funding from the insecticide
manufacturer ICI.

A lobby group that includes Bayer, Monsanto, Novartis,
Pfizer, Roche and Schering-Plough was behind the effort to discredit Purdey.
In December 1999, the same David Ray was appointed to the UK Veterinary
Products Committee (VPC) -a government body that licences animal medicines.

Purdey has been consistently denied even exploratory
funding to extend his privately supported research. Yet, the Purdey/Brown
chemical poisoning model matches with the epidermiological spread of CJD
clusters in humans. It also predicts the incidence of BSE-type diseases
in animals. The accepted infectious model does not fit either.

The pharmaceutical industry is all the more determined
to hide the chemical source of BSE and CJD, because a spotlight on chemicals
would expose the role the insecticides in Alzheimer's -another neurodegenerative
disease. That might lead to claims which would dwarf those from BSE and
CJD litigants. In fact, two leading brain researchers into CJD and Alzheimers
have died in suspicious circumstances in recent years.

In the United States, the Environmental Protection Agency
is already reviewing Phosmet's safety. The Centers for Disease control
in the US have recently conducted experiments on mice that confirm the
organophosphate risk.

Not only is the EC beef slaughter campaign futile, because
the disease is mostly non-infectious, but unless the underlying chemical
cause is addressed, BSE will simply reappear from chemical causes. A new
warble fly campaign is already underway in France using the same organophosphate
insecticide.

Of greater concern is that some lotions for scabies and
head lice are now priming children and adults, for CJD and Alzheimers in
later life.

BONDING THE PRION

Cambridge University prion biochemist, David R. Brown
is dismissive of the science behind the infectious model of BSE. He terms
it "a very limited amount of science by a few assumed- reputable scientists."
He insists there is "no evidence an infectious agent is present in
either meat or milk."

"Simple tests on udder walls of cows -which could
easily detect an infectious prion- have not been done, why I don't understand."

A number of researchers have found that organophosphate(OP)
in systemic warble fly insecticide can deform the prion molecule, rendering
it ineffective at buffering free radical effects in the body. Worse still,
the prion is then partial to bond with manganese and become a 'rogue' prion.
A chain reaction whereby rogue prions turn others to rogues also, can explain
the bovine spongiform disease mechanism.

The CJD and BSE symptoms mirror 'manganese madness',
an irreversible fatal neuro-psychiatric degenerative syndrome that plagued
manganese miners in the first half of the last century

SHINING A LIGHT ON SPONGIFORM

Organic dairy farmer and peer-review-published independent
scientist, Mark Purdey, says the accepted theory of transmission from BSE-infected
cattle to human CJD -by bonemeal or meat, is dependent on a mutant prion
that has never been isolated under the scientific protocol called Koch's
postulates.

Purdey's insistence on sticking to the letter of this
scientific law earned him the condemnation of UK officialdom when he first
mooted his theory. But Purdey pointed to CJD clusters downwind of a British
Phosmet production plant to back his case.

He gave evidence to the UK Government BSE inquiry and
was supported by Conservative MP, Thessa Gorman. His views were discounted,
but his subsequent research and the new Cambridge prion work have confirmed
the alternative theory. Despite this, and the backing of a British peer,
he is denied even exploratory funding.

Speaking from his rural English Somerset farm yesterday
-as plans forge ahead for the European cattle cull, he asks: "Why
does CJD degeneration in humans begin in the retina, and why are CJD disease
clusters found in high altitude locations?"

The question is rhetorical, and Purdey has an eye-opening
answer. He argues that the prion molecule has a known natural role as a
shock adsorber of damaging energy from ultraviolet rays and other oxidizing
agents.

Once this prion defence system is rendered ineffective
by organophosphates - for example in human head lice lotions, these oxidizing
effects have an unmediated impact on tissues. Eventually, UV radiation
damages the retina and oxidative stress destroys the brain tissues of CJD
patients. This theory would expect to find higher CJD incidence in mountain
regions -where UV radiation levels are elevated. That prediction holds
true.

A similar but accelerated mechanism could be driving
BSE. ICI's Phosmet organophosphate warble fly insecticide -applied on the
backs of animals along the spinal column, similarly degrades prions. "Systemic
versions of the insecticide are designed to make the entire cow carcass
toxic to warble fly," explains Purdey. "Unfortunately it's toxic
to prions too -especially those prions located just millimeters from the
point of application."

The damaged prions are then ready to react with manganese
in animal feed, or manganese sprayed on land or in mineral licks -to become
the driving force of BSE neurodegeneration. Purdey says manganese-tipped
prions set off lethal chain reactions that neurologically burn through
the animal.

Chickens notoriously excrete most of the supplements
fed to them -including manganese. And their manganese-rich excreta have
been blended into cattle feed in the UK. Natural variations in the relative
environmental availability of copper and manganese can also spur prion
degeneration says Purdey.

From this research, any prudent person would conclude
there is a significant risk attaching to the use of organophosphate in
humans. Preparations for head lice and scabies are known to be overused
in practice and might be priming users for CJ disease.

Purdey believes his bias for field work is the key to
his success. He bemoans the "reductionism" of much lab-centered
science. "I have traveled the world to investigate known clusters
of spongiform disease -something mainstream researchers don't seem remotely
interested in doing."

Since first postulating an environmental -rather than
infectious- theory of spongiform diseases, Purdey has built evidence from
around the world that explains and predicts the incidence in humans and
animals: a cluster of CJD in Slovakia, Eastern Europe -around a manganese
plant; Rocky Mountain deer with Chronic Wasting Disease (CWD), who were
found to be eating pine needles rich in manganese; the futile slaughter
of sheep in Cyprus -only for BSE to reemerge within years.

"The reappearance of BSE in Cyprus obviously points
to an environmental cause," says Purdey, who is sanguine when reflecting
on the condemnation of him by mainstream scientists.

"I suppose they have mortgages and kids who need
to go to university," he muses. "Privately, some were agreeing
with me, but then they would denounce me publicly. It was quite strange
really."

THE MONEY TRAIL

Critical scientists like Purdey are unlikely to prevail.
The pharma industry holds most research purse strings, and would hardly
energetically explore an avenue of research that could expose them to litigation
for causing BSE. The official theory is lavishly funded, alternative theories
rarely, if at all.

There are more explosive implications to his -and other's
latest research. Purdey says similar organophosphate-induced protein deformation
could also underlie Alzheimer's disease. If that were true, the litigation
fallout would destroy some pharmaceutical giants, and a lot of very influential
noses would be out of joint.

Disturbingly, Purdey and other brain researchers seem
to have had an undue share of unfortunate accidents. Purdey's house was
burned down and his lawyer who was working with him on Mad Cow Disease
was driven off the road by another vehicle and subsequently died. The veterinarian
on the case also died in a car crash -locally reported as: 'Mystery Vet
Death Riddle.'

Dr. C. Bruton, a CJD specialist -who had just produced
a paper on a new strain of CJD- was killed in a car crash before his work
was announced to the public. Purdey speculates that Bruton might have known
more than what was revealed in his last scientific paper.

In 1996, leading Alzheimer's researcher Tsunao Saitoh,
46 and his 13 -year-old daughter were killed in La Jolla, California, in
what a Reuters report described as a "very professionally done"
shooting.

What Alzheimer's Disease, Mad Cow Disease, and CJ Disease
have in common, is abnormal brain proteins and a putative link to organophosphates.
Even Gulf War syndrome among returning veterans has been attributed, in
part to the insecticide. But the sidelined scientists' suspicions are still
largely ignored.

In their favour at the moment, is a growing unease on
the part of the public. As BSE forges on and Governments panic, Science
may be out to lunch on BSE, compromised by bovine spongythinking myopathy.

Mark Purdey funds his own research, testing/ labs/travel
to cluster sites. Donations to his research fund will help him carry on
his work. Mark Purdey Research Fund, High Barn Farm, Elworthy, Nr Taunton,
Somerset TA4 3PX, UK.